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Aggressive Periodontitis

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Presentation on theme: "Aggressive Periodontitis"— Presentation transcript:

1 Aggressive Periodontitis
Localized & Generalized Forms

2 Aggressive Periodontitis
Common Findings: Client otherwise clinically healthy, usually < 30 years of age Characterized by rapid bone & attachment loss (inconsistent with amount of destruction) Absence of large amounts of plaque & calculus Family history – genetic trait

3 Aggressive Periodontitis
Other Findings (not universal): A.a. found in diseased sites Host response abnormalities (phagocytosis, chemotaxis) Hyperactive macrophages Produce excess amounts of prostaglandins, interleukin – 1 Disease may be self-arresting

4 Clinical Features of Localized Aggressive Periodontitis
Formerly known as localized juvenile perio Onset of disease occurs between puberty & 20 years of age Bone (3-4x faster than in chronic perio) & attachment loss affects: First molars Incisors Clinical inflammation may not be obvious Minimal plaque that rarely mineralizes However contains elevated levels of A.a. & P.g.

5 Clinical Features of Localized Aggressive Periodontitis
Maxillary incisors migrate in distolabial direction  diastema Increasing mobility of affected teeth Periodontal abscess formation Sensitive root surfaces

6 Bacterial Associated with LAP
Elevated levels of A.a. found in active sites (low numbers in healthy sites) Produce leukotoxins, collagenase, & other immunosuppressive factors that help it to evade host defense mechanisms Incidence of A.a. found to be greater in younger persons compared to older clients Younger clients experience more destruction in a shorter period of time Important to diagnosis condition in early stages

7 Site Specific Destruction
Some reasons why disease activity affects certain teeth: #1: A.a. colonize first perm. teeth to erupt Evade host defenses Following initial attack, host responds Antibodies produce which improve phagocytosis of bacteria This may prevent colonization of other sites

8 Site Specific Destruction
Additional reasons: #2: A.a. may lose its ability to produce leukotoxin This may slow or arrest the disease process #3: Antagonistic bacteria Anti-A.a. bacteria may colonize sites & prevent A.a. from colonizing other sites in mouth Localizes the infection & tissue destruction

9 Site Specific Destruction
Additional reasons: #4: Denuded root surfaces The root surfaces of clients with LAP are often denuded (absence of cementum) Allows bacteria to penetrate the root and colonize the site

10 Radiographic Evaluation
Vertical bone loss affecting: Usually bilateral affecting first permanent molars & incisors, Vertical loss of bone in an “arc-shape” extending from the distal of the 2nd premolar to the mesial of the 1st molar

11 Clinical Features of Generalized Aggressive Perio
Limited information available due to reclassification of conditions Includes conditions formerly known as gen. juvenile and rapidly progressive periodontitis Usually affects persons 30 years & younger but can affect older persons Bone & attachment loss affects at least 3 teeth other than first molars & incisors Episodic nature to disease Periods of inactivity may last weeks, months, or years

12 Clinical Features of Generalized Aggressive Perio
Often plaque is minimal but contains high levels of: A.a. P.g. F.n. & C.r. Spirochetes Episodic nature of disease produces two different tissue responses

13 Clinical Features of Generalized Aggressive Perio
Destructive phase: Tissue appears severely inflamed, ulcerated & fiery red Bleeding with or without stimulation Suppuration Active attachment & bone loss

14 Clinical Features of Generalized Aggressive Perio
Non-destructive phase: Tissues appear pink with some stippling Lack of inflammation Probing will reveal deep pockets Bone & attachment levels relatively stable

15 Associated Systemic Complications
Some clients with GAP may exhibit: Weight loss Mental depression, general malaise Systemic conditions may predispose client to GAP, these include: Chronic neutrophil defects, leukocyte adherence deficiency Functional defects of PMNs, monocytes or both  impaired chemotaxis & phagocytosis

16 Radiographic Evaluation
Severe bone loss affecting minimal number of teeth OR Majority of teeth affected by advanced bone loss

17 Prevalence of Aggressive Periodontitis
Prevalence estimates below 1% (U.S. & other countries) Prevalence for both types higher among African-Americans Gender differences unclear Distribution of disease by gender among race groups Prevalence higher for African-American males compared to females Reverse is true among whites

18 What Puts a Client at Risk?
A.a. found in large numbers in LAP A.a. produces a strong leukotoxin  kills neutrophils Different strains of A.a. produce different levels of leukotoxin Highly toxic strains produce greater numbers of leukotoxin People with the disease more likely to have highly toxic strains (African-Americans in particular)

19 Risk Defective neutrophil function another finding
Depressed neutrophil chemotaxis & phacytosis common for both forms Neutrophil dysfunction has genetic basis BUT, not all people with this dysfunction have aggressive perio AND not all people with the dysfunction have aggressive perio

20 Aggressive Periodontitis - Treatment
Depends on type and degree of destruction Aggressive forms have a poorer prognosis

21 Treatment for LAP Extraction of involved teeth (depends on severity of tissue loss) Periodontal therapy: Plaque control instruction Debridement with or without flap surgery Irrigation with CHX, home rinsing with CHX Bone grafts, root resections, hemisections Frequent maintenance visits 1/month for 6 months, then every 3 months

22 Treatment for LAP Antibiotic therapy:
Adjunctive therapy often required to eliminate A.a. from tissues Tetracycline (250 mg qid for 2 weeks) Metronidazole combined with amoxicillin Doxycycline The earlier the condition is diagnosed, the sooner tx can begin – outcome often more predictable

23 Treatment for GAP Careful monitoring of younger clients with GAP b/c rate of disease progression is often faster Maintenance every 3 weeks or less is recommended if disease in active phase Periodontal therapy: Debridement in combination with antibiotic therapy, strict plaque control, CHX irrigation & rinsing Periodontal surgery

24 Soft Tissue Management DEN4361
Treatment for GAP Antibiotic therapy: Highly recommended that microbial diagnostic & susceptibility testing be done Combination therapies include: Metronidazole/amoxicillin Amoxicillin/doxycycline Clindamycin Local therapies in the form of gels, chips or fibers (not a lot info in this area yet) Aggressive Periodontitis

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